Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “viral evolution”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1999

[Papillomavirus-induced anogenital lesions in 121 HIV seropositive men. Clinical, histological, viral study, and evolution].

OBJECTIVE: To determine the prevalence of the Human Papillomavirus (HPV) in Human Immunodeficiency Virus (HIV) infected men, using clinical examination and molecular hybridization in situ. PATIENTS AND METHODS: From May 1995 to May 1997 we studied the prevalence, clinical and histological characteristics, the types and the evolution of the HPV lesions among 121 HIV-infected men. The HPV DNA was determined by molecular hybridization in situ, using biotinylated probes which recognized HPV types 6/11, 16/18 and 31/33/35 in 79 p. 100 (5/19) of the patients (17 biopsies). RESULTS: Sixteen per cent (19/121) of the patients are HPV infected: genital warts in 37 p. 100 (7/19), anal warts in 37 p. 100 (7/19), and ano-genital warts in 26 p. 100 (5/19) of the patients. In every case of anal codyloma, intracanalar lesions were found. In 47 p. 100 (9/19) of the cases, histological exam showed an intra-epithelial neoplasia. The HPV types 6/11, 16/18 and 31/33/51 were positive in 53 p. 100 (9/17), 35 p. 100 (6/17) and 35 p. 100 (6/17) biopsies respectively. High-risk types of HPV have been noted in 71 p. 100 (12/17) of the biopsies. The evolution of the clinical lesions was: recovering in 47 p. 100 (9/19) of the patients (after 3 months of treatment), recurrence in 16 p. 100 (3/19) of the anal warts (after 1 to 3 months of treatment), stabilization in 16 p. 100 (3/19) of the genital warts (after 6 months of treatment) and extension in 11 p. 100 (2/19) of the anogenital warts (after 3 months of treatment). CONCLUSION: The high prevalence of condyloma and dysplasia emphasizes the importance of the anogenital exam in HIV-positive patients. In case of anal lesions, anuscopy and biopsy are required. We insist on the need to closely follow these patients with HPV lesions in order to adapt treatment. Anal cytology and HPV-DNA detection by Hybrid Capture Assay, should be developed for screening and prevention of the malignant transformation of HPV lesions in this population.

AIDS-Related Opportunistic Infections↗
PubMed2002

The evolution of bovine viral diarrhea: a review.

The economic importance of bovine viral diarrhea is increasing with the emergence of seemingly more virulent viruses, as evidenced by outbreaks of hemorrhagic syndrome and severe acute bovine viral diarrhea beginning in the 1980s and 1990s. It appears that evolutionary changes in bovine viral diarrhea virus were responsible for these outbreaks. The genetic properties of the classical bovine viral diarrhea virus that contribute to the basis of current diagnostic tests, vaccines, and our understanding of pathogenic mechanisms are now being reevaluated because of these "new" virus strains. This shift in virulence has confounded both nomenclature and the significance of current bovine viral diarrhea virus categorization. The purpose of this review is to summarize our current understanding of bovine viral diarrhea virus with a chronological review of prevailing scientific tenets and practices as described in clinical and scientific North American veterinary journals and textbooks. The first part of this review describes how we have arrived at our current understanding of the viruses, the diseases, and their nomenclature. The second part of the review deals with current concepts in virology and how these concepts may both explain and predict bovine viral diarrhea virus pathogenesis. By reviewing how knowledge of bovine viral diarrhea has evolved and the theories of how the virus itself is able to evolve, the interpretation of diagnostic tests are more effectively utilized in the control and treatment of bovine viral diarrhea virus associated disease.

Animals↗
PubMed1995

Evolution of the Viral Hepatitis Prevention Board.

The Viral Hepatitis Prevention Board (VHPB), an independent, international group of experts, was formed in 1992 to raise awareness about the risks of viral hepatitis and the need to prevent the disease. The VHPB's first initiative was an Action on Hepatitis B as an Occupational Hazard, under the auspices of the Society of Occupational Medicine. The objectives of this action were to increase the protection of workers at risk from infection with hepatitis B. In 1993, the VHPB widened its scope and established an Action on Hepatitis B as a Community Health Risk, under the auspices of the European Public Health Association. This action aims to inform and educate the public and policy makers about the dangers of hepatitis B, its modes of transmission and how it can be prevented in the community.

Hepatitis B↗
PubMed1998

Evolution of the Viral Hepatitis Prevention Board--VHPB.

The Viral Hepatitis Prevention Board (VHPB) was formed in 1992 to provide authoritative information and advice on hepatitis B as an occupational hazard and to act as a scientific lobby group to promote hepatitis B vaccination as part of an overall risk reduction strategy. The VHPB published Viral Hepatitis, a newsletter whose format and content was designed to appeal to both professional and lay readers seeking information on hepatitis. The VHPB was successful in lobbying the European Parliament to add the Code of Practice on Vaccination to legislation protecting workers from occupationally acquired infections. The first initiative on occupational hepatitis B culminated in an international congress in March 1993 and the publication of 'Hepatitis B as an Occupational Hazard' in the WHO occupational health series. Since 1993 the Board has discussed HBV as a community acquired infection; control of hepatitis A (HAV) and eligibility for hepatitis A vaccine and combined hepatitis A and B vaccines; hepatitis C; and reviewed progress towards the control of HBV and the adoption of universal vaccination programmes in countries of low endemicity. A major international congress in Cannes in November 1993 took stock of actions taken to control hepatitis B as a community health risk in industrialised countries. The constitution and membership of the Board underwent significant change at the end of 1994. A Secretarial was located within the Centre for the Evaluation of Vaccination at the University of Antwerp to deal with all administrative matters and publications in peer reviewed journals. The format of Viral Hepatitis was re-focused to increase the scientific content. The Board extended its actions geographically in 1996 to include the countries of Central and Eastern Europe (CEE) and the Newly Independent States (NIS) of the former Soviet Union. The success of the VHPB has exceeded all the expectations of the founding members. The major focus of the annual programme of meetings and of publications remains on hepatitis B and its prevention through vaccination. But more and more the broad range of prevention and control strategies for all forms of hepatitis is dealt with.

Europe↗
PubMedDate not supplied

Viral myocarditis. Clinical, electrocardiographic and evolutive diversity.

Five observations of severe viral myocarditis are presented. Diverse cardiac emergencies (pump failure, ventricular premature beats or tachycardia, left bundle branch block, trifascicular block, grade 2 or 3 a-v block, severe hypotension, etc.) as well as associated conditions (pericarditis, interstitial nephritis, pneumonia, pulmonary massive thromboembolism) could be found. The course of the disease was acute in three cases, subacute in one and chronic in another. Two patients died with severe pump failure (associated with pulmonary thromboembolism in one case), The clinical, evolutive and histologic aspects were in good correlation. These cases illustrate the clinical, electrocardiographic and evolutive diversity of viral myocarditis.

Adult↗
PubMed2000

Baseline HIV type 1 genotypic resistance to a newly added nucleoside analog is predictive of virologic failure of the new therapy.

We evaluated the predictive value of baseline HIV-1 genotypic resistance mutations for failure of a nucleoside reverse transcriptase inhibitor (NRTI) containing therapy. The change in therapy of 88 HIV-1-infected patients was analyzed retrospectively, relating the genotypic resistance profile at baseline to the evolution of viral load and CD4+ T cell counts. Genotypic resistance at baseline and at 6 months was evaluated with the LiPA HIV-1 RT, which detects mutations at codons 41, 69, 70, 74, 184, and 215. At 1 to 3 months after change in therapy, patients without preexisting resistance mutations to the new drug (group S) had a significantly better evolution in viral load (reduction of 0.37 log(10)) compared with patients with known preexisting resistance mutation(s) (group R) (increase of 0.08 log(10)). This difference was particularly striking for patients with the baseline M184V mutation and whose treatment was modified by the addition of lamivudine. After 6 months the median difference in viral load evolution between the two groups increased to 0.61 log(10): the viral load of patients of group S was still 0.18 log(10) below baseline while patients of group R had an increase of 0.43 log(10) in viral load above baseline. Changes in CD4+ T cell counts were not significantly different. The evolution in viral load in HIV-1-infected patients with and without baseline resistance mutation(s) toward a newly added NRTI is significantly different at 1-3 months and at 6 months after changing or adding one NRTI.

CD4 Lymphocyte Count↗
PubMed2005

Antigenic stimulation specifically reactivates the replication of archived simian immunodeficiency virus genomes in chronically infected macaques.

Human immunodeficiency virus/simian immunodeficiency virus (SIV) diversification is a direct consequence of viral replication and occurs principally in secondary lymphoid organs where CD4(+) T cells are activated and proliferate. However, the evolution of viral quasispecies may also be driven by various nonexclusive mechanisms, including adaptation to specific immune responses and modification of viral fitness. Analysis of viral quasispecies in SIV-infected macaques subjected to repeated antigenic stimulations allowed us to demonstrate transient expansions of SIV populations that were highly dependent upon activation of antigen-specific T cells. T-cell clones expanded in response to a particular antigen were infected by a specific viral population and persisted for prolonged periods. Upon a second stimulation by encounter with the same antigen, these specific genomes were at the origin of a new burst of replication, leading to rapid but transient replacement of the viral quasispecies in blood. Finally, longitudinal analysis of SIV sequence variation during and between antigenic stimulations revealed that viral evolution is mostly constrained to periods of strong immunological activity.

Amino Acid Sequence↗
PubMed2004

Similar HIV-1 evolution and immunological responses at 10 years despite several therapeutic strategies and host HLA Types.

Two sexual partners infected with related HIV-1 viruses and enrolled in different therapeutic strategies including structured treatment interruptions (STI) provided us an opportunity to compare long term (10 years) viral genetic evolution for closely related isolates in different hosts. HLA loci were molecularly typed and different genetic markers were studied. The viral genetic evolution was studied by sequencing pol and env genes. The HIV-specific CD4+ and CD8+ T cell responses were assessed by the lymphoproliferative response (LPR) and an ELISPOT assay, respectively. HLA class I loci of patients A and B were different and both of them were heterozygous for CCR5delta32 gene. During the two STI studies, viral load of both patients rebounded after treatment interruption and both developed a transitory strong helper and CTL responses. After definitive interruption of therapy, viral load remained below 5,000 copies/ml without therapy during the two years of follow-up. Two patients infected with related viruses showed a similar dynamics of viral evolution and CD4 T cells, despite hosts having a different HLA type and being treated with several therapeutic protocols, after 10 years of infection. These results suggest that, in this case, an effective immunological response to STI depended more on the virus than on the characteristics of the host.

Anti-HIV Agents↗
PubMed2004

On the role of RNA silencing in the pathogenicity and evolution of viroids and viral satellites.

Viroids and most viral satellites have small, noncoding, and highly structured RNA genomes. How they cause disease symptoms without encoding proteins and why they have characteristic secondary structures are two longstanding questions. Recent studies have shown that both viroids and satellites are capable of inducing RNA silencing, suggesting a possible role of this mechanism in the pathology and evolution of these subviral RNAs. Here we show that preventing RNA silencing in tobacco, using a silencing suppressor, greatly reduces the symptoms caused by the Y satellite of cucumber mosaic virus. Furthermore, tomato plants expressing hairpin RNA, derived from potato spindle tuber viroid, developed symptoms similar to those of potato spindle tuber viroid infection. These results provide evidence suggesting that viroids and satellites cause disease symptoms by directing RNA silencing against physiologically important host genes. We also show that viroid and satellite RNAs are significantly resistant to RNA silencing-mediated degradation, suggesting that RNA silencing is an important selection pressure shaping the evolution of the secondary structures of these pathogens.

Base Sequence↗
PubMed2006

Infectious molecular clones from a simian immunodeficiency virus-infected rapid-progressor (RP) macaque: evidence of differential selection of RP-specific envelope mutations in vitro and in vivo.

A minor fraction of simian immunodeficiency virus (SIV)-infected macaques progress rapidly to AIDS in the absence of SIV-specific immune responses. Common mutations in conserved residues of env in three SIVsmE543-3-infected rapid-progressor (RP) macaques suggest the evolution of a common viral variant in RP macaques. The goal of the present study was to analyze the biological properties of these variants in vitro and in vivo through the derivation of infectious molecular clones. Virus isolated from a SIVsmE543-3-infected RP macaque, H445 was used to inoculate six naive rhesus macaques. Although RP-specific mutations dominated in H445 tissues, they represented only 10% of the population of the virus stock, suggesting a selective disadvantage in vitro. Only one of these macaques (H635) progressed rapidly to AIDS. Plasma virus during primary infection of H635 was similar to the inoculum. However, RP-specific mutations were apparently rapidly reselected by 4 to 9 weeks postinfection. Terminal plasma from H635 was used as a source of viral RNA to generate seven full-length, infectious molecular clones. With the exception of one clone, which was similar to SIVsmE543-3, clones with RP-specific mutations replicated with delayed kinetics in rhesus peripheral blood mononuclear cells and human T-cell lines. None of the clones replicated in monocyte-derived or alveolar macrophages, and all used CCR5 as their major coreceptor. RP variants appear to be well adapted to replicate in vivo in RP macaques but are at a disadvantage in tissue culture compared to their parent, SIVsmE543-3. Therefore, tissue culture may not provide a good surrogate for replication of RP variants in macaques. These infectious clones will provide a valuable reagent to study the roles of specific viral variants in rapid progression in vivo.

Amino Acid Sequence↗
PubMed1997

Nutrition and newly emerging viral diseases: an overview.

Infectious diseases are on the increase worldwide. When discussing interactions of nutrition and infection, nutritionists have traditionally considered only the effects of diet on the host. Recent data, however, indicate that, at least for an RNA virus, host nutriture can influence the genetic make-up of the pathogen and thereby alter its virulence. This symposium was organized to alert the nutrition community to this discovery and its possible implications for the investigation of nutrition-infection interrelationships. Topics covered in the symposium include the following: the public health threat of emerging viral diseases; the rapid evolution of viral RNA genomes; oxidants and antioxidants in viral diseases-disease mechanisms and metabolic regulation; and increased virulence of coxsackievirus B3 due to vitamin E or selenium deficiency. If the findings with coxsackievirus are more broadly applicable to other RNA viruses, the results could be of great public health significance because RNA viruses constitute the majority of all plant, animal and human viruses.

Antioxidants↗
PubMed1998

Lack of evidence of a stable viral load set-point in early stage asymptomatic patients with chronic HIV-1 infection.

OBJECTIVE: To address the question of whether individuals with chronic HIV-1 infection have a stable viral load set-point and to assess the influence of host and viral factors on the evolution of viral load in a subset of stable asymptomatic patients with a baseline viral load below 5000 copies/ml and CD4+ T-cell count above 500 x 10(6)/l. METHODS: Medical visits were performed at least every 6 months including routine blood analysis, viral load and CD4+ T-cell count. HIV-1 RNA was measured in frozen (-70 degrees C) plasma samples using PCR. Patients were classified into three groups according to baseline viral load: group A, < 200 copies/ml (undetectable); group B, 201-2000 copies/ml; group C, 2001-5000 copies/ml. A survival analysis and a Cox regression model were performed to assess the influence of viral and host factors in the increase of baseline viral load. The endpoint was the time to increase viral load to a stable level > 0.5 log10 copies/ml above baseline viral load in groups B and C and to a stable detectable viral load (> 200 copies/ml) in group A. RESULTS: A cohort of 114 patients with viral load below 5000 copies/ml was followed for a median of 12 months (6-42 months). Overall, 22 (19%) out of 114 patients had an increase > 0.5 log10 copies/ml of baseline viral load. Baseline viral load increased in two (5%) out of 37 patients in group A, four (12%) out of 33 patients in group B, and 16 (36%) out of 44 patients in group C (survival analysis, P<0.002). Patients of group C had a eightfold higher risk of increasing baseline viral load than patients in the other two groups pooled together (hazards ratio, 8.28; 95% confidence interval, 1.78-38; P = 0.006). Patients with an increase of viral load to the virological endpoint had a threefold higher risk of decreasing baseline CD4+ T-cell counts > 100 x 10(6)/I than patients with stable viral load (hazards ratio, 2.78; 95% confidence interval, 1.12-14; P = 0.03). CONCLUSIONS: In our cohort of chronically HIV-1-infected asymptomatic patients with a baseline viral load < 5000 copies/ml and CD4+ cell count > 500 x 10(6)/l, a true viral load set-point did not seem to exist. Patients with baseline viral load of 2000-5000 copies/ml had an eightfold higher risk of increasing the level of viral load than patients with a baseline viral load below 2000 copies/ml.

Adult↗